Proliferative retinopathies are a classification of diseases that include sickle cell retinopathy, diabetic retinopathy, branch vein occlusion retinopathy, and retinopathy of prematurity. An interesting paradox in these retinopathies is that the hypoxia in the retina triggers growth of blood vessels in the vitreous but not in the retina itself. If we could identify the mechanism of this inhibition we may be able to temporarily suppress the inhibition and stimulate vessel growth within the retina. In order to develop strategies to prevent proliferative retinopathies we must understand the changes in gene expression that are responsible for disease progression. We propose to utilize proteomics and DNA-microarrays to identify differential expressed genes between normal retinas and retinas from two mouse models of proliferative retinopathy. The proposed experiments will determine the gene expression profile of the retinas during the course of these disease models. We anticipate that such knowledge will significantly increase our understanding of human retinopathy of prematurity. Some of the differentially expressed proteins are likely to be essential regulators for normal retinal vascular development, while other proteins may be inhibitors of vascular development. By identifying new candidate proteins, this project would feed into our long-range goals of identifying proteins that are essential regulators of retinal vascular development.